Pathologic vertebral fractures result in pain and disability in a large population of patients with trabacular bone deficiencies. Increasing life expectancy of cancer patients allowing skeletal metastatic and myeloma progression and aging of the general population is expected to lead to a significant increase in the at risk population. We hypothesize that the lack of accurate and reliable clinical predictors of fracture risk in pathologic vertebrae is due to a lack of understanding of the underlying mechanisms. We further hypothesize that the underlying mechanism is the accumulation of a critical level of damage (microcracking) in trabecular bone. Thirdly, we hypothesize that the damage accumulation process is different in diffuse loss of bone versus focal loss of bone, leading to different levels of fracture risk at a given loss of bone mass. Our long term goal is to better understand and thereby better manage the clinical problem of pathologic vertebral fractures. As a first step, we propose to develop a Finite Element Analysis (FEA) model to investigate the damage accumulation process in vertebral trabacular bone. We will develop a model of trabecular bone behavior including damaging effects with material parameters derived from cyclic creep tests of vertebral bone specimens. This material model will be implemented within a FEA model to predict the response of vertebral trabecular bone specimens to leading (tension, compression, torsion). These predictions will be compared with experimental results from mechanical tests of vertebral trabecular specimens. "Pathologic" conditions will be investigated using FEA models of specimens with "high" or "low" densities and cylindrical osteolytic defects under loading. Mechanical testing of specimens with "high" and "low" apparent densities and stimulated defects will be used to examine the analytical predictions. These examinations of the effects of damage accumulation on the material behavior of vertebral trabacular bone will provide significant information on trabacular bone behavior. More importantly, it will provide the basis for further investigations towards the overall goal of interpreting non-invasive clinical measures of trabecular bone adequacy to determine long-term likelihood of pathologic vertebral fracture.